Pneumonias acquired in the community are the form of pneumonia most often seen in the offices of general practitioners, private radiologists, and in a hospital setting, in the outpatient department or the emergency room. Most CAP patients are children (15–35 of 1,000 children per year) and the elderly (30–40 per 1,000 persons per year). The mode of transmission in CAP is usually person-to-person, via water or mucus droplets laden with viruses or bacteria. The most frequent pathogens are gram-positive bacteria, such as Streptococcus pneumoniae (Pneumococcus) and Staphylococcus aureus, and gram-negative bacteria, such as Haemophilus influenzae and atypical bacteria, including Mycoplasma pneumoniae, Chlamydia pneumoniae, and Legionella pneumophila. Viral forms commonly include those caused by respiratory viruses, such as influenza viruses, human metapneumovirus, respiratory syncytial virus (RSV), rhinovirus, parainfluenza viruses, adenoviruses, and corona viruses. According to the literature, the spectrum of organisms varies according to patient-related, temporal, geographic, and diagnostic factors.

In CAP, the patient’s health and socioeconomic status may provide clues as to the spectrum of causative organisms. Healthy people are most likely to contract mycoplasma pneumonia or a mild form of pneumococcal pneumonia. Debilitated patients, alcoholics, and the chronically ill more often present with severe pneumococcal pneumonia or infections caused by H. influenzae, S. aureus, or gram-negative bacilli. L. pneumophila and Chlamydia infections are more common in patients with some form of mild immunologic compromise. Patients with poor oral hygiene and occasional loss of consciousness (epilepsy, alcoholism) may suffer from anaerobic pulmonary infections. In these patients, Mycobacterium tuberculosis infections are more prevalent than in healthy individuals without risk factors. Recurrent pneumonia in outpatients usually indicates an underlying problem, such as congenital or acquired immunologic disorder; airway abnormalities, such as chronic bronchitis, bronchiectasis, and bronchogenic carcinoma; cardiac conditions (congestive heart failure); or systemic diseases, such as diabetes, chronic alcoholism, and intravenous drug abuse. Up to 10% of CAPs are aspiration pneumonias caused by the aspiration of colonized oropharyngeal or gastric contents. The most frequently isolated pathogens in aspiration pneumonia are gram-negative bacteria. Aspiration pneumonia must be differentiated from aspiration pneumonitis, which is a chemical pneumonitis that results from the aspiration of noncolonized gastric contents (Mendel-son’s syndrome).

The definition of CAP has been challenged over the last few years, as it also includes pneumonia in patients from nursing homes, rehabilitation hospitals, and outpatient-based surgical centers who routinely receive invasive medical treatment. The bacteriology and outcome of these patients are more similar to those of NPs. Therefore, it has been proposed that pneumonia in outpatients hospitalized for more than 2 days over the previous 3 months or who reside in nursing homes or extended-care facilities should be categorized as health-care-associated pneumonia (HCAP).

Patients suffering from CAP usually present with fever, cough, dyspnea, sputum production, and pleuritic chest pain, as well as laboratory signs, such as leukocytosis. Because the clinical symptoms are nonspecific, most people who have fever and cough do not have pneumonia; in fact, about 30% of patients, and especially the elderly, are afebrile at presentation. Imaging is one of the most important tools in the diagnosis of CAP. The radiographic identification of a new pulmonary infiltrate is, in the appropriate clinical setting, indicative of pneumonia. Conversely, a patient who has fever and cough but does not have radiologic proof of pneumonia cannot be considered to have pneumonia. In CAP, the causative organism is frequently not identified because noninvasive tests such as sputum cultures correctly identify the offending organism in only 50% of cases, and invasive procedures are rarely used in patients with pneumonia.

In patients with CAP, the primary role of the radiologist is to detect or to exclude pneumonia. A second task is to aid the clinician in determining the etiologic diagnosis. Categorization of the causative organism is sometimes possible by integrating clinical and laboratory information with radiographic pattern recognition (see the section “Radiographic Patterns”). A specific etiologic diagnosis, however, is difficult to establish, given the increasing spectrum of causative organisms and their overlapping radiographic features. In a prospective study of 359 adults with CAP, Fang and coauthors compared the radiographic, clinical, and laboratory features of patients with bacterial pneumonia (caused by H. influenzae, S. pneumoniae, S. aureus, and aerobic gram-negative bacilli) and those with atypical pneumonia (caused by M. pneumoniae and Chlamydia spp.). The authors found no features that could reliably differentiate these two groups. Another group prospectively compared the clinical and radiologic features of CAP caused by L. pneumophila to those of patients with pneumococcal infections AUHA (Ahuja and Kanne, 2014). The authors concluded that Legionella infection may clinically as well as radiologically resemble a typical bacterial pneumonia.

The chest radiogram is the first-line tool in evaluating patients with suspected CAP. Computed tomography (CT) is reserved for assessing complications or for guiding further diagnostic procedures. It is definitely indicated in investigating patients with recurrent or persistent pulmonary opacifications.

By definition, NPs develop in a hospital environment. The incidence of NP ranges from 0.5 to 5 cases per 100 admissions, but in the subgroup of ventilated patients in an intensive care setting it may reach 7–41%. Mortality rates reported for NPs range from 20% in multihospital studies to ⩾50% in single referral centers and university hospitals.

Mortality is related to the causative agent. The prognosis associated with aerobic gram-negative pneumonias is considerably worse than that associated with gram-positive or viral agents.

NP develops from bacterial colonization of the oropharynx followed by the aspiration of oropharyngeal secretions and gastrointestinal contents into the lungs. The majority of NPs are caused by gram-negative bacilli, including Pseudomonas aeruginosa, Klebsiella spp., Enterobacteriaceae spp., Escherichia coli, Serratia marcescens, and Proteus, and to a lesser extent by gram-positive cocci, atypical bacteria such as L. pneumophila, and viruses such as RSV. Microbial contamination of inserted tubes, lines, and catheters is an important source of infection. Less commonly, NP is the result of bacteremia originating from right-sided endocarditis or septic pelvic thrombophlebitis. Risk factors are either patient-related (underlying illness, previous surgery, prolonged hospital care) or iatrogenic (intravascular catheters, tracheal tubes, indwelling catheters, respirator equipment). Sources of infections are hospital personnel and patients with active infections. The inappropriate use of broad-spectrum and prophylactic antibiotics is an additional and important factor leading to an increased susceptibility to NPs.

Compared with CAP, it may be difficult for the clinician to diagnose pneumonia in a hospitalized patient. The classical findings for pneumonia, such as new fever, new pulmonary opacification on chest radiographs, cough, sputum production, and elevated leukocyte count may not be present in the hospitalized patient with NP. Moreover, even if these symptoms are present, they may not necessarily be caused by pneumonia. Microbiologic evaluation of the patient with suspected NP (sputum, bronchoalveolar lavage) may or may not be helpful because of the difficulties in differentiating contamination from true infection. In addition, pulmonary disease in a hospital environment may be caused by more than one agent. Therefore, identifying a pulmonary infection, the various methods used to obtain a specimen, and the value of isolating potential pathogens are matters of constant discussion in the clinical diagnosis of NP.

Because of the potential difficulties in the clinical diagnosis of pneumonia in the hospitalized patient, the radiologist has an important role in detecting and classifying suspected cases. However, the radiographic diagnosis of a pulmonary opacity in suspected NP is not as straightforward as it is in patients with CAP. The radiographic diagnosis of a pneumonia may be hampered by preexisting disorders or concomitant lung disease, such as fibrosing alveolitis, lupus pneumonitis, hemorrhage or contusion, acquired respiratory distress syndrome (ARDS), tumor, atelectasis, and embolic infarcts. These disorders may obscure or alter the otherwise characteristic radiographic appearance of a pulmonary opacification and thus render the etiologic approach using pattern recognition difficult.

The difficulties in diagnosing NP can be readily demonstrated by two examples. Winer-Muram et al. assessed the diagnostic accuracy of bedside chest radiography for pneumonia in ARDS patients. The overall diagnostic accuracy in these patients was only 42% because of false-negative and false-positive results originating from diffuse parenchymal areas of increased opacity that obscured the radiographic features of pneumonia. Wunderink et al. compared premortem chest radiographic findings with pulmonary autopsy studies in ventilated patients with NP. No radiographic sign had a diagnostic efficiency greater than 68%. The only radiographic sign that correlated with pneumonia, correctly predicting 60% of the cases, was the presence of an air bronchogram.

CT is used more often when an NP is suspected than in patients with CAP, as it can detect early morphologic signs of infection (for example, ground-glass densities). CT can also identify a pulmonary opacification in areas of preexistent disease, detect complications, and guide invasive diagnostic procedures, such as bronchoscopy or percutaneous biopsy.

In general terms, imaging patterns can be grouped into airspace consolidation (lobar pneumonia), bronchiolar disease (bronchopneumonia) and bilateral diffuse disease.

Most commonly, consolidation, confined to a segment or a lobe of one or both lungs, is caused by typical and atypical bacteria, whereas bronchopneumonia commonly relates to Staphylococcus aureus, Haemophilus, Mycoplasma, and tuberculous infection. Diffuse bilateral lung disease, frequently developing over time, can in most cases be attributed to viruses and fungi such as Pneumocystis jirovecii. Nodular disease may be attributed to septic emboli (small nodules), larger nodules can be caused by Nocardia and fungal disorders in immunocompromised hosts.

Again, these patterns are nonspecific, they overlap, may be mimicked by non-infectious lung disease and masked by pre- or coexisting lung conditions. Patterns can be identified both on chest radiography and CT but CT may help to identify complex or coexisting patterns and aid the novice in establishing a diagnosis.

Since the first description of HIV/acquired immune deficiency syndrome (AIDS), Pneumocystis pneumonia caused by Pneumocystis jirovecii (PJP) has been one of its most common complications. (Previously it was thought that Pneumocystis carinii was the cause of these infections, but this is not the case. The abbreviation PCP is still used in some circles to refer to Pneumocystis pneumonia.) In recent years the incidence of PJP as a presenting abnormality in patients with AIDS has decreased. Nevertheless it still accounts for a considerable amount of diseases in patients not on highly active antiretroviral therapy (HAART) or prophylactic therapy and should be considered as a diagnosis when characteristic radiographic findings are noted. Patients with PJP typically present with increasing shortness of breath; the disease may run a gradual or fulminant course. Chest films classically reveal a bilateral fine to medium reticulonodular pattern, generally bilateral but occasionally focal or unilateral. If the patient remains untreated, the radiograph progressively becomes more opaque and bilateral homogeneous opacities may ultimately be seen. While upper lobe involvement is more frequent, any lobe may be involved. On CT imaging PJP presents as ground-glass opacification in the areas of involvement, typically perihilar in distribution. The chest film occasionally may worsen within a few days of intravenous trimethoprim-sulfamethoxazole treatment secondary to overhydration and the production of pulmonary edema, but this can be treated quite effectively with diuretics.

Otherwise, with treatment, the radiographic course is one of steady improvement, with complete resolution usually occurring by day 11. Pneumatoceles, as seen on chest films, develops in 5⩾10% of patients; the incidence is probably higher in patients evaluated by CT scanning. These air-filled cysts are frequently multiple, located in the upper lobes, measure 1–5 cm in diameter, and will resolve within 2 months. However, in 35% of patients, pneumatoceles may lead to pneumothorax, which can be extremely difficult to treat. Overall, pneumothorax develops in 5% of patients with PJP and AIDS. In about 10% of patients with PJP, the chest film may be normal. In some of these patients with normal radiographs, a CT scan will show the typical geographic, ground-glass opacities associated with Pneumocystis pneumonia. Lymphadenopathy and pleural effusions are not part of the PJP picture.

Cytomegalovirus (CMV) may mimic the appearance of PJP on chest film, with diffuse bilateral fine to medium reticulonodular opacities. On CT, centrilobular nodules and ground-glass opacities are reported. In some patients with CMV, the presence of discreet nodules, sometimes several centimeters in size, may help distinguish between these two entities. Lymphocytic interstitial pneumonia may also mimic PJP with fine reticular opacities on chest radiographs, ground-glass opacities on CT scans, and air-filled cysts seen on both forms of imaging.

Disseminated fungal infections, such as histoplasmosis and coccidiomycosis, generally produce bilateral, fairly symmetric, coarse, nodular opacities on chest radiographs.

The nodules and occasionally reticular opacities are larger than those seen with PJP, which may aid in distinguishing between the two processes. Discreet larger nodule(s) or disseminated disease may be seen with other fungal infections such as aspergillosis and cryptococcosis. With angio-invasive fungal infections cavitation may occur secondary to ischemia, regardless of the CD-4 lymphocyte count.

The imaging appearance of tuberculosis (TB) depends on the patient’s immune status. In patients with relatively normal CD-4 lymphocyte cell counts, TB will look much like it does in the general population. That is, with primary infection, patients will present with a homogeneous lobar opacity and ipsilateral hilar and/or mediastinal adenopathy. With post-primary infection, chest films will show apical and posterior upper-lobe and/or superior segment lower-lobe heterogeneous opacities with or without cavitation; on CT scans, imaging may also demonstrate centrilobular nodules and/or tree-in-bud opacities. In patients with low CD-4 cell counts and primary infection, homogeneous lobar opacities with adenopathy similar to immune competent hosts may be seen on chest films, but increased adenopathy may also be present. With post-primary disease, the organism disseminates more widely, creating a diffuse, coarse, nodular pattern on chest film similar to the pattern seen with fungal infections. Cavitation does not develop, as the body’s immune response is weak, such that well-formed granulomas and necrosis are unusual. In patients with improving cell-mediated immunity secondary to HAART, more typical findings of cavitation might be seen. If the organism is sensitive to the appropriate therapy, then some resolution of the abnormal findings should be observed on chest film within 1 week.

Ordinary bacterial infections now occur with increased frequency and among some patients with HIV are the most common type of infection. This increasing percentage of bacterial infections may reflect the larger number of pulmonary infections in populations in whom antiretroviral and prophylactic therapy is available. Common organisms are S. pneumoniae, H. influenzae, S. aureus, and P. aeruginosa. In the immunocompromised, pneumonias caused by these bacteria usually appear as they do in normal hosts, i.e., as homogeneous, peripheral, lobar opacities. Parapneumonic effusions may be present. S. aureus, and P. aeruginosa pneumonias may present with cavitations. These should begin to resolve within days of instituting antibacterial therapy, with complete resolution of abnormalities usually occurring in about 2 weeks. Other bacterial etiologies, such as Rhodococcus equi and Nocardia asteroides, are less common and may present as nodules or masses with or without cavitation.

With the use of antiretroviral therapy, noninfectious etiologies of disease have become more prevalent, such as pulmonary hypertension and chronic obstructive pulmonary disease (COPD), including emphysema and chronic bronchitis. Also, the immune reconstitution inflammatory syndrome (IRIS), occurring in up to 30% of patients after the initiation of antiretroviral treatment, may cause confusing clinical and radiological findings. With improving immune status, patients are able to mount a greater inflammatory response to existing organisms, resulting in worsening clinical disease and increasing lung parenchymal abnormalities and lymphadenopathy. This usually develops in individuals with low CD-4 counts and high viral loads, typically about one month after starting therapy (but as early as within days and as late as after several months). It is more commonly seen in patients with partially treated tuberculosis or non-tuberculous mycobacterial infection. Worsening of other infections and the development of sarcoidosis have also been attributed to HAART and IRIS.